Evidence map›Paper›PMID 35055131›Full record

ArticleInternational journal of molecular sciences2022

Common and Distinctive Intercellular Communication Patterns in Human Obstructive and Nonobstructive Hypertrophic Cardiomyopathy.

Christina J Codden, Michael T Chin

Open access · goldAbstract readComparative Study
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Insights into the Structural and Proteomic Changes inAnimals : an open access journal from MDPI · 2025
    Article
  7. Article
  8. Review
  9. Single Cell Transcriptomic Profiling ofJournal of the American Heart Association · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Genetic and Molecular Mechanisms of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023
    Article
  16. Review
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Christina J CoddenMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.
Michael T ChinMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.ORCID 0000-0003-3065-8498
Tufts Medical Center · US

Funding

Tufts Clinical and Translational Science Institute (Pilot Supplement)UL1TR002544 · NCATS · TUFTS UNIVERSITY BOSTON · PI SELKER, HARRY P. · 2018 to 2022
$50.2M
American Heart Association 18IPA34170294NCATS NIH HHS UL1TR002544
6 · The paper itself

Abstract

Hypertrophic Cardiomyopathy (HCM) is a common inherited disorder characterized by unexplained left ventricular hypertrophy with or without left ventricular outflow tract (LVOT) obstruction. Single-nuclei RNA-sequencing (snRNA-seq) of both obstructive and nonobstructive HCM patient samples has revealed alterations in communication between various cell types, but no direct and integrated comparison between the two HCM phenotypes has been reported. We performed a bioinformatic analysis of HCM snRNA-seq datasets from obstructive and nonobstructive patient samples to identify differentially expressed genes and distinctive patterns of intercellular communication. Differential gene expression analysis revealed 37 differentially expressed genes, predominantly in cardiomyocytes but also in other cell types, relevant to aging, muscle contraction, cell motility, and the extracellular matrix. Intercellular communication was generally reduced in HCM, affecting the extracellular matrix, growth factor binding, integrin binding, PDGF binding, and SMAD binding, but with increases in adenylate cyclase binding, calcium channel inhibitor activity, and serine-threonine kinase activity in nonobstructive HCM. Increases in neuron to leukocyte and dendritic cell communication, in fibroblast to leukocyte and dendritic cell communication, and in endothelial cell communication to other cell types, largely through changes in the expression of integrin-β1 and its cognate ligands, were also noted. These findings indicate both common and distinct physiological mechanisms affecting the pathogenesis of obstructive and nonobstructive HCM and provide opportunities for the personalized management of different HCM phenotypes.

Indexed as

Gene Regulatory NetworksCardiomyopathy, HypertrophicCell CommunicationComputational BiologyDatabases, GeneticGene Expression ProfilingGene Expression RegulationHumansHypertrophy, Left VentricularMaleSequence Analysis, RNASingle-Cell AnalysisVentricular Outflow Obstructiondendritic cellsHypertrophic Cardiomyopathyintegrin-β1left ventricular outflow tract obstructionsingle-nucleus RNA-sequencing

Identifiers

PMID35055131
PMCPMC8780670
OpenAlexW4225920775

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.